CCL20-CCR6 axis modulated traumatic brain injury-induced visual pathologies

Area of Science:

• Neuroscience
• Immunology
• Ophthalmology

Background:

• Traumatic brain injury (TBI) is a significant cause of death and disability globally.
• Repetitive TBI (rTBI) in athletes can lead to cumulative neurological effects, including visual impairment.
• The CCL20-CCR6 axis is implicated in neuroinflammation and neurodegeneration following TBI.

Purpose of the Study:

• To investigate the role of the CCL20-CCR6 signaling pathway in mediating visual dysfunction after rTBI.
• To explore potential therapeutic interventions targeting this axis.

Main Methods:

• Mice (wild type and CCR6 knockout) were subjected to closed head rTBI.
• Mice were treated with pioglitazone (PPARγ agonist) or anti-CCL20 antibody.
• Histopathological analysis assessed cerebral and retinal pathologies, and inflammatory changes.

Main Results:

• rTBI induced neurodegeneration, retinal damage, and inflammation, with increased CCL20 expression.
• CCR6 knockout mice exhibited reduced retinal degeneration and inflammation.
• CCL20 neutralization and pioglitazone treatment decreased CCL20, retinal damage, and inflammation.

Conclusions:

• The CCL20-CCR6 axis plays a significant role in rTBI-induced retinal pathology.
• Targeting the CCL20-CCR6 pathway may offer a therapeutic strategy for visual dysfunction following rTBI.